ArlR regulates environmental stress tolerance and biofilm formation in foodborne Staphylococcusaureus
TL;DR
It is demonstrated that deletion of arlR significantly reduces the tolerance of the foodborne strain RMSA49 to acetic acid, desiccation, whereas its responses to temperature and osmotic stress not affected, and that the arlR mutant also exhibits significantly enhanced biofilm formation.
Abstract
Staphylococcus aureus (S. aureus) is a major Gram-positive pathogen capable of sensing and responding to diverse host- and environment-derived stresses, contributing to both clinical infections and foodborne illnesses. This exceptional stress tolerance is primarily mediated by intricate regulatory networks. Although the ArlRS two-component system is known to regulate autolysis, capsule synthesis, and virulence, the specific role of ArlR in environmental stress adaptation remains poorly understood. In this study, we demonstrate that deletion of arlR significantly reduces the tolerance of the foodborne strain RMSA49 to acetic acid, desiccation, whereas its responses to temperature and osmotic stress not affected. Notably, the arlR mutant also exhibits significantly enhanced biofilm formation. Transcriptomic analysis, validated by RT–qPCR, further reveals that ArlR regulates a broad set of stress- and biofilms-associated genes, highlighting its central role in coordinating environmental adaptation. These findings establish ArlR as a key regulator of environmental stress adaptation in foodborne S. aureus RMSA49 and suggest its potential as a target for controlling S. aureus.